{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,21]],"date-time":"2026-05-21T02:54:36Z","timestamp":1779332076505,"version":"3.51.4"},"reference-count":35,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,11,11]],"date-time":"2005-11-11T00:00:00Z","timestamp":1131667200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Developmental Dynamics"],"published-print":{"date-parts":[[2006,2]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>The <jats:italic>Tgif<\/jats:italic> gene encodes a homeodomain protein that functions as a transforming growth factor beta (TGF\u2010\u03b2) repressor by binding to Smad2. Mutations in the <jats:italic>TGIF<\/jats:italic> gene are associated with human holoprosencephaly, a common birth defect caused by the failure of anterior ventral midline formation. However, Smad2\u2010mediated TGF\u2010\u03b2 signaling in the axial mesendoderm has been demonstrated to be essential for ventral midline formation, and loss of a Smad2 antagonist should in principle promote rather than inhibit ventral midline formation. This suggests a more complex mechanism for the function of TGIF in controlling ventral midline formation. To explore the role of TGIF in ventral forebrain formation and patterning, we investigated <jats:italic>Tgif<\/jats:italic> expression and function during mouse development by in situ hybridization and gene targeting. We found that <jats:italic>Tgif<\/jats:italic> is highly expressed in the anterior neural plate, consistent with the proposed neural differentiation model in which TGF\u2010\u03b2 suppression is required for normal neural differentiation. This result suggests a possible role for <jats:italic>Tgif<\/jats:italic> in anterior neural differentiation and patterning. However, targeted disruption of the <jats:italic>Tgif<\/jats:italic> gene during mouse development does not cause any detectable defects in development and growth. Both histological examination and gene expression analysis showed that <jats:italic>Tgif<\/jats:italic><jats:sup>\u2212\/\u2212<\/jats:sup> embryos have a normal ventral specification in the central nervous system, including the forebrain region. One interpretation of these results is that the loss of TGIF function is compensated by other TGF\u2010\u03b2 antagonists such as c\u2010Ski and SnoN during vertebrate anterior neural development. Developmental Dynamics 235:547\u2013553, 2006. \u00a9 2005 Wiley\u2010Liss, Inc.<\/jats:p>","DOI":"10.1002\/dvdy.20642","type":"journal-article","created":{"date-parts":[[2005,11,16]],"date-time":"2005-11-16T17:49:38Z","timestamp":1132163378000},"page":"547-553","source":"Crossref","is-referenced-by-count":27,"title":["Expression and functional analysis of <i>Tgif<\/i> during mouse midline 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